TY - JOUR
T1 - Variation in Listeria monocytogenes dose responses in relation to subtypes encoding a full-length or truncated internalin A
AU - Chen, Yuhuan
AU - Ross, William H.
AU - Whiting, Richard C.
AU - van Stelten, Anna
AU - Nightingale, Kendra K.
AU - Wiedmann, Martin
AU - Scott, Virginia N.
N1 - Funding Information:
From the Department of Medicine (HMP), Washington University School of Medicine, St. Louis, Missouri; Department of Medicine (WDH), Emory University School of Medicine, Atlanta, Georgia: Family Practice (JRB). Cedar Rapids, Iowa; Department of Pharmacology (DWB), University of Illinois College of Medicine at Rockford. Rockford, Illinois; Department of Medicine (JBK), University of Medicine and Dentistry of New Jersey, New Brunswick, New Jersey; Department of Internal Medicine (RRT), University of Texas Medical Branch at Galveston, Galveston, Texas; and Glaxo Inc. Research Institute (DLD, AP. MS), Research Triangle Park, North Carolina. This work was supported by a grant from Glaxo Inc. Research Institute. Research Triangle Park, North Carolina. Requests for reprints should be addressed to H. Mitchell Perry, Jr.. M.D.. Hypertension Division, Washington University School of Medicine, Box 8048, 660 South Euclid, St. Louis, Missouri 63110. Manuscript submitted October 22,1992, and accepted in revised form April 5, 1993.
PY - 2011/2
Y1 - 2011/2
N2 - Internalin A (InlA; encoded by inlA) facilitates the crossing of the intestinal barrier by Listeria monocytogenes. Mutations leading to a premature stop codon (PMSC) in inlA and thus attenuated mammalian virulence have been reported. We recently characterized 502 L. monocytogenes food isolates from a retail survey and 507 human clinical isolates from multiple U.S. states with respect to the presence/absence of inlA mutations. The objective of this study was to investigate the hypothesis that dose responses for human listeriosis vary between L. monocytogenes strains with and those without a PMSC in inlA. Subtype-specific prevalence and concentration distributions in food, along with epidemiologic and consumption data, were input into established doseresponse models to generate an r value (probability of a cell causing illness). Under the conservative assumption that L. monocytogenes levels at retail represent levels consumed, mean log10 r values were -8.1 and -10.7 for L. monocytogenes subtypes with genes encoding a full-length and a truncated InlA, respectively. L. monocytogenes carrying a 5' frameshift mutation in a homopolymeric tract showed a mean log10 r value of -12.1. Confidence intervals for the r values and their differences varied depending on subtypes. When the increase in concentration of L. monocytogenes subtypes between retail and consumption was considered, mean log10 r values were reduced to -10.4, -13.8, and -12.8 for the subtypes with genes encoding a full-length InlA, for the subtypes carrying a PMSC in inlA, and for all L. monocytogenes isolates regardless of subtype, respectively. Our study provides further quantitative evidence that L. monocytogenes subtypes vary in abilities and relative likelihoods of causing human disease, which were mechanistically related to defined genetic markers.
AB - Internalin A (InlA; encoded by inlA) facilitates the crossing of the intestinal barrier by Listeria monocytogenes. Mutations leading to a premature stop codon (PMSC) in inlA and thus attenuated mammalian virulence have been reported. We recently characterized 502 L. monocytogenes food isolates from a retail survey and 507 human clinical isolates from multiple U.S. states with respect to the presence/absence of inlA mutations. The objective of this study was to investigate the hypothesis that dose responses for human listeriosis vary between L. monocytogenes strains with and those without a PMSC in inlA. Subtype-specific prevalence and concentration distributions in food, along with epidemiologic and consumption data, were input into established doseresponse models to generate an r value (probability of a cell causing illness). Under the conservative assumption that L. monocytogenes levels at retail represent levels consumed, mean log10 r values were -8.1 and -10.7 for L. monocytogenes subtypes with genes encoding a full-length and a truncated InlA, respectively. L. monocytogenes carrying a 5' frameshift mutation in a homopolymeric tract showed a mean log10 r value of -12.1. Confidence intervals for the r values and their differences varied depending on subtypes. When the increase in concentration of L. monocytogenes subtypes between retail and consumption was considered, mean log10 r values were reduced to -10.4, -13.8, and -12.8 for the subtypes with genes encoding a full-length InlA, for the subtypes carrying a PMSC in inlA, and for all L. monocytogenes isolates regardless of subtype, respectively. Our study provides further quantitative evidence that L. monocytogenes subtypes vary in abilities and relative likelihoods of causing human disease, which were mechanistically related to defined genetic markers.
UR - http://www.scopus.com/inward/record.url?scp=79953214600&partnerID=8YFLogxK
U2 - 10.1128/AEM.01564-10
DO - 10.1128/AEM.01564-10
M3 - Article
C2 - 21169442
AN - SCOPUS:79953214600
SN - 0099-2240
VL - 77
SP - 1171
EP - 1180
JO - Applied and environmental microbiology
JF - Applied and environmental microbiology
IS - 4
ER -